With this assumption, an enhanced firing of CCK and SST cells in our model will ultimately enhance the release of neurotransmitter GABA, and since CCK and SST cells are specialized to fine-tune and provide dendritic inhibition to CA1 pyramidal cells, perhaps this overdrive of inhibitory function in early stages of AD is a protective mechanism, preventing CA1 pyramidal cell hyperexcitability that is shown to develop at midstages of the disease (Petrache et al. 2019), developing at ~ 6 months and correlating with a decline in CCK and SST cell function probably due to exocytotic death. The gene discussed is SST; the disease is Alzheimer disease.